Evidence map›Paper›PMID 40593443›Full record

ArticleMolecular biology reports2025

CALR regulates the proliferation and drug sensitivity of multiple myeloma cells through the BCL2 signaling pathway.

Yin Wang, Xiaoli Hu, Yaqi Song, Qianqi Ruan, Xiaoteng Bai, Juan Du

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Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Yin Wang *Department of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China.
Xiaoli Hu *Department of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China.
Yaqi Song *Department of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China.
Qianqi RuanDepartment of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China.
Xiaoteng BaiThe First Clinical Medical College, Lanzhou University, Lanzhou, 730099, China.
Juan DuDepartment of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China. juan_du@live.com.

Funding

National Natural Science Foundation of China 82370206, 82170198
6 · The paper itself

Abstract

backgroundCalreticulin (CALR) has been implicated in the genesis and progression of numerous tumors. Nevertheless, its impact on multiple myeloma (MM) remains ambiguous. This study aimed to explore the effect of CALR on the proliferation and drug sensitivity of MM cells and to delve into its underlying mechanism.

methodsFirst, the expression of CALR in MM cells was measured. Subsequently, the impact of CALR knockdown on MM cells was validated both in vitro and in vivo. Finally, RNA sequencing was utilized to explore the molecular mechanisms associated with CALR knockdown.

resultsWe determined that CALR is upregulated in myeloma cells. Both in vitro and in vivo functional assays demonstrated that CALR knockdown attenuated the proliferative capacity of MM cells, heightened their sensitivity to bortezomib (BTZ), and facilitated MM cell apoptosis. RNA-sequencing results indicated that CALR knockdown activates the apoptosis pathway, with the underlying mechanism potentially involving the regulation of the BCL2 signaling pathway.

conclusionThis study indicates that CALR is associated with the proliferation and drug sensitivity of MM. Targeting CALR might be a potential strategy to further enhance the treatment efficacy for MM. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

CalreticulinMultiple MyelomaProto-Oncogene Proteins c-bcl-2AnimalsAntineoplastic AgentsApoptosisBortezomibCell Line, TumorCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMiceSignal TransductionXenograft Model Antitumor AssaysAntineoplastic AgentsBCL2 protein, humanBortezomibCalreticulinCALR protein, humanProto-Oncogene Proteins c-bcl-2ApoptosisBCL2CalreticulinMultiple myelomaProliferation

Identifiers

PMID40593443

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.